L-deprenyl inhibits tumor growth, reduces serum prolactin, and suppresses brain monoamine metabolism in rats with carcinogen-induced mammary tumors

Previously, we have reported that L-deprenyl decreased the incidence of mam mary tumors and pituitary tumors in old acyclic rats, The objective of the present study was to investigate the effects of L-deprenyl, a monoamine oxi dase-B (MAO-B) inhibitor, treatment on the development and growth of tumors and on the metabolism of catecholamines and indoleamine in the medial basa l hypothalamus (MBH) and the striatum (ST) of rats bearing 7,12-dimethylben zanthracene (DMBA)-induced mammary tumors, Female Sprague-Dawley rats with DMBA-induced mammary tumors were injected (sc) daily with 0.25 mg or 5.0 mg of deprenyl/kg BW or the vehicle (saline; control) for 12 wk. Tumor diamet er, tumor number, body weight, and feed intake were measured every week of the treatment period. Serum PRL and the concentrations of catecholamines, i ndoleamine, and their metabolites were measured by RIA and HPLC, respective ly, Treatment with 5.0 mg deprenyl decreased the tumor diameter, tumor numb er, and serum prolactin (PRL) level. Although the body weight increased in all three groups, the body weight gain in the 5.0 mg group was smaller than that in the control and 0.25 mg groups. Deprenyl treatment had no effect o n feed intake. The concentrations of dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were decreased in the MBH and the ST, and the conc entration of 5-hydroxy-indoleacetic acid (5-HIAA) was decreased in the MBH of deprenyl-treated rats. Treatment with 5.0 mg deprenyl enhanced the conce ntrations of norepinephrine (NE) and serotonin (5-HT) in the MBH and in the ST, and the concentration of dopamine (DA) in the MBH. These results sugge st that the suppression of the development and growth of DMBA-induced mamma ry tumors by chronic deprenyl treatment may be mediated through alterations in the synthesis and metabolism of catecholamines and indoleamine in the M BH and inhibition of PRL secretion.